Complement Activation by β-Amyloid in Alzheimer Disease

Alzheimer disease (AD) is characterized by excessive deposition of the β-amyloid peptide (β-AP) in the central nervous system. Although several lines of evidence suggest that β-AP is neurotoxic, a mechanism for β-AP toxicity in AD brain remains unclear. In this paper we provide both direct in vitro evidence that β-AP can bind and activate the classical complement cytolytic pathway in the absence of antibody and indirect in situ evidence that such actions occur in the AD brain in association with areas of AD pathology.